Gene Expression of Matrix Metalloproteinases in Clara-Cell Secretory Protein-Deficient Mice Exposed to Cigarette Smoke

Abstract

Clara-cell secretory protein (CCSP) is thought to play a role as a regulator of inflammatory response. To investigate how CCSP plays a role in lung remodeling induced by exposure to cigarette smoke, we examined gene expression of matrix metalloproteinases (MMPs) and chemokine mRNA in lungs of mice exposed to cigarette smoke. CCSP-deficient (CCSP-/-) strain 129 and wild-type (WT) strain 129 mice were exposed to sidestream cigarette smoke for 4 h/day, for 4 wk. Expression of MMP-2, MMP-9, interleukin-10 (IL-10), and macrophage inflammatory protein-2 (MIP-2) mRNA in lungs was measured by reverse-transcription polymerase chain reaction (RT-PCR) using p-actin as an internal standard to quantify PCR amplification of mRNA. No significant differences were observed in gene expression of MMP-2, MMP-9, IL-10, and MIP-2 mRNA between CCSP-/- and wild-type mice exposed to cigarette smoke. This suggests that CCSP is not correlated with cigarette smoke-induced pulmonary response through MMPs and chemokines.